Key result
Antiplatelet resistance post-stroke is multifactorial, linked to drug interactions, comorbidities, and CYP2C19 polymorphisms.
Why the study?
Many patients develop resistance to antiplatelet drugs after atherothrombotic ischemic stroke, but there is no gold standard method to determine high residual platelet activity.
This review highlights the complex interplay of clinical, pharmacological, and genetic factors contributing to antiplatelet resistance in ischemic stroke patients, emphasizing the potential need for personalized secondary prevention strategies.
May guide personalized secondary prevention after ischemic stroke; leaves open prospective trials to confirm utility of genetic testing.
Every year, 20 % of all ischemic strokes are recurrent, characterized by severe course and high mortality and disability rates. Secondary prevention measures are aimed at preventing repeated brain catastrophes, which leads to a 20–30 % reduction in the risk of recurrent stroke. One of the directions of therapy is the appointment of antiplatelet drugs. Currently, acetylsalicylic acid and clopidogrel are widely used in the Russia. Effective platelet inhibition by prescribing these antiplatelet agents is one of the priorities in the treatment of atherothrombotic ischemic stroke. At the same time, a number of patients develop resistance to antiplatelet agents, which is associated with a variety of factors, such as drug interactions, concomitant diseases, and genetic predisposition. In order to control the formation of laboratory resistance, several methods for assessing platelet function have been developed. For example, optical Born aggregatometry, thromboelastogram, flow cytometry. Currently, there is no “golden method” for determining the high residual activity of platelets, since none of them has achieved a significant advantage. This article discusses methods for detecting laboratory resistance and factors influencing its development, depending on the prescribed antiplatelet drug.
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Batenkova et al. (2025) conducted a review in Ischemic stroke. Antiplatelet therapy (acetylsalicylic acid and clopidogrel) was evaluated. Resistance to antiplatelet therapy after ischemic stroke is multifactorial and associated with drug interactions, concomitant diseases, and genetic polymorphisms such as CYP2C19.
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